ライフサイエンスコーパス: tangle

1 gous and nonhomologous partners ("chromosome tangles").

2 th increased risk for AD and neurofibrillary tangles.

3 opposite to the female excess of plaques and tangles.

4 t knit together to form a mesh of disordered tangles.

5 aques and tau-immunoreactive neurofibrillary tangles.

6 ia, AD, neuritic plaques, or neurofibrillary tangles.

7 leading to the formation of neurofibrillary tangles.

8 e intracellular formation of neurofibrillary tangles.

9 at the expense of increasing neurofibrillary tangles.

10 ks: amyloid-beta plaques and neurofibrillary tangles.

11 rate amyloid-beta plaques or neurofibrillary tangles.

12 eta (Abeta) peptides for plaques and tau for tangles.

13 sease before the accumulation of plaques and tangles.

14 od vessels, and formation of neurofibrillary tangles.

15 roportional to the number of neurofibrillary tangles.

16 teractions and accumulate in neurofibrillary tangles.

17 amyloid angiopathy (CAA) and neurofibrillary tangles.

18 bsence of amyloid plaques or neurofibrillary tangles.

19 in rates of global cognitive decline as did tangles.

20 mation of senile plaques and neurofibrillary tangles.

21 gregates into characteristic neurofibrillary tangles.

22 oteins, and Tau, which forms neurofibrillary tangles.

23 of amyloid beta (Abeta) and neurofibrillary tangles.

24 s: amyloid abeta1-42 and Tau neurofibrillary tangles.

25 loid (Abeta) plaques and tau neurofibrillary tangles.

26 arkers of senile plaques and neurofibrillary tangles.

27 threads and neurofibrillary tangles and pre-tangles.

28 nal transport independently from plaques and tangles.

29 e model of AD that develops both plaques and tangles (3xTg).

30 au leads to the formation of neurofibrillary tangles, a hallmark of Alzheimer disease (AD), and relat

31 hosphorylated tau protein in neurofibrillary tangles, a process that occurs late in the disease proce

32 we first assessed the patterns of brain tau tangle accumulation (measured with the positron emission

33 While plaque and tangle accumulation likely contributes to neuron and syn

34 tions are observed through colocalization in tangle aggregates in the Alzheimer's disease (AD) brain.

35 Tau tangle aggregation in this region may develop concurrent

36 ase (AD) is characterized by neurofibrillary tangles, amyloid plaques, and neurodegeneration.

37 er) and pathologic burden of neurofibrillary tangles, amyloid plaques, vascular lesions, and Lewy bod

38 expression levels were associated with Braak tangle and Braak plaque scores, with elevated expression

39 h age, presence of infarcts, neurofibrillary tangle and neuritic plaque scores, APOE epsilon4 allele

40 ase (AD) is characterized by neurofibrillary tangle and neuropil thread deposition, which ultimately

41 co-localized with phosphorylated tau in pre-tangle and tangle-bearing neurons.

42 g, flexible physical filaments are naturally tangled and knotted, from macroscopic string down to lon

43 ervations of the patterns of neurofibrillary tangles and amyloid plaques in Alzheimer's disease sugge

44 ven without Abeta.SIGNIFICANCE STATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key lesions

45 n precedes the appearance of neurofibrillary tangles and contributes to neuronal loss.

46 otein (APP), and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphor

47 brains (eg, intraneuronal and extraneuronal tangles and dystrophic neurites), but does not seem to b

48 eactivity is associated with neurofibrillary tangles and is involved in tau degradation.

49 d with thioflavin-S-positive neurofibrillary tangles and less reactive in neuropil threads and extrac

50 Tau immune-reactive neurofibrillary tangles and neuritic threads were present in the cerebra

51 re abnormal at old age (7-9 months) when tau tangles and neurodegeneration are extensive.

52 ng) pathological inclusions, neurofibrillary tangles and neuropil threads but only in the patient who

53 gs] pathological inclusions, neurofibrillary tangles and neuropil threads.

54 ection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neuri

55 au inclusions in the form of neurofibrillary tangles and Pick bodies and in some cases glial Tau path

56 Recently, tangles and plaque-like aggregates have been identified

57 form of neuropil threads and neurofibrillary tangles and pre-tangles.

58 es were accompanied by the resolution of tau tangles and significantly decreased neurodegenerative pa

59 the first appearance of amyloid plaques and tangles and the manifestation of dementia is now well es

60 marks of the disease such as neurofibrillary tangles and widespread neuronal losses.

61 cting incidental age-related neurofibrillary tangles) and neuromelanin-containing neurons in the subs

62 hology (neuritic plaques and neurofibrillary tangles) and the interval between time of testing and ti

63 a hierarchical vulnerability of neurons for tangles, and a widespread nonspecific pattern of plaques

64 altered Tau phosphorylation, neurofibrillary tangles, and accumulation of insoluble protein plaques.

65 he densities of Lewy bodies, neurofibrillary tangles, and aminergic neurons in the locus ceruleus, do

66 amyloid (Abeta) plaques, tau neurofibrillary tangles, and cognitive deficits, suggesting that it cont

67 from detecting these species before plaques, tangles, and cognitive impairment become evident and fro

68 atter damage, brain atrophy, neurofibrillary tangles, and dementia.

69 -amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and TAR DNA-binding

70 nts and was associated with amyloid plaques, tangles, and hippocampal sclerosis but not neocortical L

71 After controlling for amyloid plaques, tangles, and hippocampal sclerosis, TDP-43 pathology was

72 (Abeta)-containing plaques, neurofibrillary tangles, and neuronal loss in the brain.

73 myloid-beta (Abeta) plaques, neurofibrillary tangles, and reactive gliosis.

74 e X chromosome was nearly always involved in tangles, and small autosomes were involved more often th

75 rrelate with the accumulation of plaques and tangles, and they are a direct consequence of the damage

76 llmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss.

77 of swollen and collapsed t-ts, patches of SR tangling, and disorder with rearrangement of the mitocho

78 Amyloid plaques and tau tangles are common pathological hallmarks for Alzheimer'

79 thology, density of neuronal neurofibrillary tangles, area occupied by amyloid-beta plaques, and the

80 n of extracellular plaques and intracellular tangles as playing a fundamental role in the course and

81 uce hyperphosphorylated tau, neurofibrillary tangles as well as aberrant amyloid precursor protein pr

82 , neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction.

83 the mammalian target of rapamycin (mTor) in tangle-bearing neurons in AD brains and its role in the

84 eemed to correlate with the terminal zone of tangle-bearing neurons in some instances.

85 he active form of mTor per se accumulates in tangle-bearing neurons, particularly those at early stag

86 ed with phosphorylated tau in pre-tangle and tangle-bearing neurons.

87 , less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% CI, -1.52 to -0.0

88 id plaques and intraneuronal neurofibrillary tangles, both of which comprise highly insoluble, densel

89 -negative" subjects have low neurofibrillary tangle Braak stages.

90 FAs with neuritic plaque and neurofibrillary tangle burden as well as domain-specific cognitive perfo

91 ossibility that knowledge of neurofibrillary tangle burden in the presence of moderate or frequent pl

92 Cerebral neurofibrillary tangles burden, in addition to alpha-synuclein pathology

93 develops amyloid plaques and neurofibrillary tangles but also because it enabled us to explore whethe

94 athology literature, which suggests that tau tangles but not amyloid-beta plaques correlate with cogn

95 ation or amyloid beta (by ELISA); plaques or tangles (by immunohistochemistry); or brain volume loss

96 ary constituent of Alzheimer neurofibrillary tangles, can form liquid droplets and therefore has the

97 io, and hippocampal volume), neurofibrillary tangles (cerebrospinal fluid phosphorylated tau181 assay

98 Amyloid plaques and neurofibrillary tangles co-occur in Alzheimer disease, but with differen

99 e (AD) include intraneuronal neurofibrillary tangles composed of abnormally hyperphosphorylated tau p

100 myloid-beta peptide leads to neurofibrillary tangles composed of aggregated hyperphosphorylated tau.

101 ike dementia associated with neurofibrillary tangles composed of hyperphosphorylated microtubule-asso

102 Abeta) in brain is linked to neurofibrillary tangles composed of hyperphosphorylated tau in AD.

103 Neurofibrillary tangles, composed of hyperphosphorylated tau fibrils, ar

104 re and a neuritic component; neurofibrillary tangles, composed predominantly of hyperphosphorylated t

105 ic brain frequently exhibits neurofibrillary tangles comprised of aggregates of the protein tau.

106 rotein aggregates, including neurofibrillary tangles comprised of tau in Alzheimer's disease and Lewy

107 abundant amyloid plaques and neurofibrillary tangles concurrent with synaptic and neuronal loss, is t

108 erphosphorylated tau (pTau), neurofibrillary tangle conformational-epitope (cNFT), amyloid-beta, astr

109 yloid beta (Abeta)-protein and intracellular tangles containing hyperphosphorylated Tau protein.

110 pment of amyloid plaques and neurofibrillary tangles contributes to neuronal loss.

111 typical AD--on the basis of neurofibrillary tangle counts in hippocampus and cortex and ratio of hip

112 Neurofibrillary tangle counts were performed using thioflavin-S microsco

113 opment, whereas in liquid crystals transient tangled defect lines were observed during isotropic-nema

114 ct of the epsilon4 allele on neurofibrillary tangle density (interaction estimate, -0.42; SE = 0.17;

115 dependently associated with an increased tau tangle density (p = 4.9 x 10(-4) ), an increased burden

116 hasic case displayed higher right-hemisphere tangle density despite greater left-hemisphere hypoperfu

117 g AD pathology (Braak score, Abeta load, and tangle density) and directly with performance in episodi

118 associated with paired helical filament tau tangle density, and the expression of BIN1 was associate

119 of global Alzheimer pathology, amyloid load, tangle density, macroscopic infarcts, microinfarcts, and

120 d among persons with AD dementia, and PHFtau tangle density.

121 , Abeta load and paired helical filament tau tangle density.

122 amyloid-beta plaque and tau neurofibrillary tangle deposition, neuroinflammation is considered a key

123 ts presence in intraneuronal neurofibrillary tangle deposits, where it takes the form of aggregated p

124 y, unsynapsed chromosome segments trapped in tangles displayed an elevated density of DSB markers lat

125 e data suggest that amyloid-beta plaques and tangles do not inevitably result in neural system derang

126 2) is critically important for resolving DNA tangles during cell division, and as such, it is a broad

127 that this tilt assists DNA spooling without tangling during packaging.

128 vated PSK is associated with neurofibrillary tangles, dystrophic neurites surrounding neuritic plaque

129 The Tangle-Entropy (TS) plots show the strong preservation o

130 tions among these elements and highlight the tangled evolutionary relationships within the phageome.

131 ) with high affinity for tau neurofibrillary tangles, excellent selectivity against Abeta plaques, an

132 o occurs in quantum wavefunctions, where the tangled filaments are vortices (nodal lines/phase singul

133 pathological tau species and neurofibrillary tangles following a single dose of AAV-vectored PHF1 com

134 d-beta deposition, neuroinflammation and tau tangle formation all play a significant role in Alzheime

135 abnormal tau aggregation, which may promote tangle formation and accelerate the development of AD pa

136 sease (AD) in regard to both neurofibrillary tangle formation and neuronal network hyperexcitability.

137 r injections induced AD-type neurofibrillary tangle formation in the macaque brain.

138 Remarkably, cell death was dissociated from tangle formation in this natural 3D model of AD.

139 ion of amyloid-beta (Abeta), neurofibrillary tangle formation, and a microglial-driven inflammatory r

140 Amyloid deposition, tangle formation, neuroinflammation and neuronal dysfunc

141 milial neurodegeneration and neurofibrillary tangle formation.

142 genomes of protists are subject to the most tangled forms of gene expression yet identified.

143 x precedes the spread of tau neurofibrillary tangles from the limbic areas to the cortex.

144 its strand-passaging activity that resolves tangled genomic DNA during mitosis.

145 zed by amyloid-beta plaques, neurofibrillary tangles, gliosis, and neuronal loss.

146 of Alzheimer's disease (AD; neurofibrillary tangles) had its first foothold in specific parts of the

147 eding of amyloid fibrils and neurofibrillary tangles has been invoked to explain the stereotypical sp

148 tomography tracers targeting neurofibrillary tangles has enabled the distribution of tau pathology to

149 ecently, PET tracers for tau neurofibrillary tangles have become available and have shown utility in

150 ed in Tau clearance, showing that even after tangles have formed, Tau-dependent behavioral and synapt

151 from in vivo imaging of neurofibrillary tau tangles have not yet been explored.

152 of Alzheimer's disease (AD) with plaques and tangles (i.e., 3xTg mice).

153 e which elucidates the evolution of a vortex tangle in a superfluid, requires an in-depth understandi

154 phorylated and deposits into neurofibrillary tangles in AD.

155 in Tau, a major component of neurofibrillary tangles in Alzheimer disease and other tauopathies.

156 451 or (18) F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessi

157 dies in Parkinson's disease, neurofibrillary tangles in Alzheimer's disease, polyQ inclusions in expa

158 isk of AD and development of neurofibrillary tangles in APOE epsilon4+ individuals.

159 antly in the EC that the formation of mature tangles in old mice was associated with excitatory cell

160 e disease characterized by deposition of tau tangles in the brain are highly susceptible to developin

161 le inclusion bodies known as neurofibrillary tangles in the brain tissue of patients with a variety o

162 oid-beta (Abeta) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunctio

163 oid beta (Abeta) plaques and neurofibrillary tangles in the brain.

164 the accumulation of amyloid plaques and tau tangles in the brain.

165 pocampal-sparing AD has more neurofibrillary tangles in the cortex and fewer in the hippocampus, wher

166 are characterized by the formation of mature tangles in the entorhinal cortex and disorientation and

167 l perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy aff

168 Neuropathological data indicate that tau tangles in the medial temporal lobe (MTL) underlie episo

169 active in neuropil threads and extracellular tangles in TPSD and FAD.

170 laques) and the tau protein (neurofibrillary tangles) in the brains of affected individuals.

171 ta-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer disease (AD).

172 tion with senile plaques and neurofibrillary tangles is a major feature of several neurodegenerative

173 ouse model of AD, which develops plaques and tangles later in its life cycle, was bred with IL-1beta(

174 The tau tangle ligand (18)F-AV-1451 ((18)F-T807) binds to neurom

175 Multiple U1 snRNP subunits form cytoplasmic tangle-like structures in AD but not in other examined n

176 All three antibodies stained tangle-like structures in different brain sections of TH

177 of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with clinical progressio

178 is, blocked amyloid formation, and decreased tangle load in the brain.

179 alyses, global Alzheimer pathology, amyloid, tangles, macroscopic infarcts, and neocortical Lewy bodi

180 have long demonstrated that neurofibrillary tangles made of hyperphosphorylated tau proteins are clo

181 u22 mice, the development of neurofibrillary tangles made of mutant human tau was not accelerated in

182 rmations of tau suggests a potential role in tangle maturation and, thus, could serve as a useful bio

183 st range of timescales and are governed by a tangled network of molecular interactions.

184 to assess the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synuclein inclusions, a

185 d time interaction terms for neurofibrillary tangles, neuritic plaques, gross infarcts, microinfarcts

186 pathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts, cystic infarct

187 age point these mice exhibit neurofibrillary tangles, neurodegeneration and cognitive deficits.

188 leading to the formation of neurofibrillary tangles, neurodegeneration, and the symptom of dementia.

189 reologically-based counts of neurofibrillary tangles, neurons and reactive glia, and morphological an

190 tain non-amyloid-plaque, non-neurofibrillary-tangle neuropathologies.

191 protein accumulation drives neurofibrillary tangle (NFT) formation in several neurodegenerative dise

192 ased tau phosphorylation and neurofibrillary tangle (NFT) formation in vivo, the molecular link assoc

193 amyloid plaque deposits and neurofibrillary tangle (NFT) formation, resulting in cognitive impairmen

194 relation to Abeta plaque and neurofibrillary tangle (NFT) pathology during disease onset is unknown.

195 The study used Braak neurofibrillary tangle (NFT) stage, frequency of neuritic plaques, and L

196 associated with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer neuritic plaques,

197 Abeta) plaques or tau-filled neurofibrillary tangles (NFT), is considered the most predictive patholo

198 protein (Abeta) plaques and neurofibrillary tangles (NFT).

199 ggregation of tau protein in neurofibrillary tangles (NFTs) (1, 2).

200 density and distribution of neurofibrillary tangles (NFTs) and amyloid-rich neuritic plaques.

201 ta plaques (NP tau), AD-like neurofibrillary tangles (NFTs) and neuropil threads (NTs).

202 Neurofibrillary tangles (NFTs) are the pathological hallmark of neurodeg

203 se (AD) is very distinctive: neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau selec

204 ve diseases characterized by neurofibrillary tangles (NFTs) comprising filamentous tau protein.

205 basalis (NB) neurons display neurofibrillary tangles (NFTs) during Alzheimer's disease (AD) progressi

206 f hyperphosphorylated tau in neurofibrillary tangles (NFTs) is a neuropathological hallmark of tauopa

207 auopathies, characterized by neurofibrillary tangles (NFTs) of phosphorylated tau proteins, are a gro

208 ty and neocortical spread of neurofibrillary tangles (NFTs) with clinical AD disease progression offe

209 Neurofibrillary tangles (NFTs), a marker of neuronal alterations in Alzh

210 oligomers, which form before neurofibrillary tangles (NFTs), are the true neurotoxic tau entities in

211 Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphory

212 Neurofibrillary tangles (NFTs), hippocampal sclerosis, lacunar infarcts,

213 ology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported that cyclin-depende

214 protein that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheimer's disease (AD

215 The formation of neurofibrillary tangles (NFTs), oxidative stress and neuroinflammation h

216 ve diseases characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheim

217 -existing tau aggregates and neurofibrillary tangles (NFTs), which are associated in AD and tauopathi

218 by a pathological hallmark: neurofibrillary tangles (NFTs).

219 levels were associated with neurofibrillary tangles (NFTs).

220 tau-null background, these mice had similar tangle numbers but were protected against neurotoxicity.

221 d with Parkinson disease and neurofibrillary tangles observed in Alzheimer disease.

222 s (PHFs) that constitute the neurofibrillary tangles observed in neuronal cell bodies in individuals

223 zero-temperature limit consists of a dynamic tangle of quantized vortex filaments.

224 halmoscopic examination revealed an abnormal tangle of vessels and enlarged draining veins.

225 lding and aggregation as the neurofibrillary tangles of Alzheimer's disease, whereas OGlcNAcylation s

226 bundles of noncrossing axons flanking large tangles of midline glial processes.

227 ular interactions are initiated by insoluble tangles of phosphorylated tau protein and plaques of amy

228 Tangles of string typically become knotted, from macrosc

229 ransition metal ions and the neurofibrillary tangles of Tau protein.

230 as plaques and intracellular neurofibrillary tangles of tau protein.

231 Neurofibrillary tangles, one of the hallmarks of Alzheimer disease (AD),

232 They include Alzheimer disease, tangle-only dementia, Pick disease, argyrophilic grain d

233 ive diseases, including Alzheimer's disease, tangle-only dementia, Pick disease, argyrophilic grain d

234 kage, shunts, abnormal vessel branching, and tangles) or the posterior pole (hyperfluorescent lesions

235 However, besides plaques and tangles, other biochemical and morphological features ar

236 frequency of Alzheimer-type neurofibrillary tangles (p < 0.05).

237 4) ), an increased burden of neurofibrillary tangles (p = 9.1 x 10(-3) ), and an increased rate of co

238 ogy (NIA ADC, Braak stage of neurofibrillary tangles, p = 3.9 x 10-6, and Consortium to Establish a R

239 ignificantly associated with neurofibrillary tangle pathology (P = .01352 and .03151, respectively);

240 Abeta40, Abeta38, sAPPalpha, and sAPPbeta), tangle pathology (P-tau), blood-brain-barrier function (

241 ing P301Ltau-overexpressing mice with severe tangle pathology and neurodegeneration.

242 patients with AD and severe neurofibrillary tangle pathology and were accompanied by changes in the

243 howed a strong association with risk for AD, tangle pathology, and global cognitive decline (p = 2.67

244 These findings suggest that tangle pathology, hippocampal sclerosis, TDP-43 and perf

245 ng may promote or accelerate neurofibrillary tangle pathology, we explored the effect of recombinant

246 his is insufficient in accelerating neuritic tangle pathology.

247 ignificantly reduced phospho-tau species and tangle pathology.

248 disease, including distinct neurofibrillary tangle pathology.

249 cident AD and development of neurofibrillary tangle pathology.

250 erbates hallmark amyloid and neurofibrillary tangle pathology.

251 included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Asses

252 oid plaques (Pearson r = -0.48; P < .01) and tangles (Pearson r = -0.55; P = .01) in the brain.

253 examine the anatomical consequences of early tangles, plaques, or the combination.

254 in argyrophilic grain disease (AGD; n = 5), tangle-predominant senile dementia (TPSD; n = 5), Pick d

255 ease interneuronal plaques and intraneuronal tangles, presently observed aberrations in hyperinsuline

256 x flows generated by vortex rings and vortex tangles (quantum turbulence).

257 e disease-senile plaques and neurofibrillary tangles-ramify systematically through the brain.

258 e to form senile plaques and neurofibrillary tangles, respectively, are induced to misfold and self-a

259 ading to amyloid plaques and neurofibrillary tangles, respectively, which are histopathological hallm

260 ly correlated with tau hyperphosphorylation, tangles score and Braak stage in human brain.

261 associations of cerebral tau neurofibrillary tangles score with the interval between onset of motor a

262 luble and associate with Tau neurofibrillary tangles selectively in Alzheimer disease (AD).

263 aberrant mitotic spindle with disorganized, tangle-shaped microtubules and reduced aster formation,

264 dividual was also assigned a neurofibrillary tangle stage (B1-B3), relating to the likelihood of havi

265 orrespondence of Thal amyloid phase to Braak tangle stage and ante-mortem clinical characteristics in

266 having Alzheimer's disease (neurofibrillary tangle stage B1; n=37).

267 having Alzheimer's disease (neurofibrillary tangle stage B2; n=56), those with hippocampal TDP-43 ha

268 having Alzheimer's disease (neurofibrillary tangle stage B3; n=205), those with hippocampal TDP-43 h

269 contrast, Thal amyloid phase, but not Braak tangle stage or cerebral amyloid angiopathy predicted (1

270 -Pittsburgh compound B values, but not Braak tangle stage or cerebral amyloid angiopathy.

271 nd all assigned Thal amyloid phase and Braak tangle stage using thioflavin-S fluorescent microscopy.

272 mer's disease severity, as measured by Braak tangle stage, and correlated with amyloid-beta42 and amy

273 hases were older at death, had a lower Braak tangle stage, and were less frequently APOE-epsilon4 pos

274 Alzheimer's disease cases, showed that Braak tangle stage, but not Thal amyloid phase predicted age a

275 We found that knowledge of neurofibrillary tangle stage, modeled as the sort of information that co

276 e-mortem clinical status was driven by Braak tangle stage.

277 amyloid angiopathy, and determined the Braak tangle stage.

278 uate the effect of different neurofibrillary tangle stages on the rates of progression on several sta

279 of amyloid-beta plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decli

280 maintain the division plane identity factor TANGLED (TAN) after PPB disassembly, although POK1 and T

281 tau protein aggregates into neurofibrillary tangles that progressively spread to synaptically connec

282 phenotype of a mouse model with plaques and tangles, the triple-transgenic mice.

283 onents of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheime

284 d outline the principles of knot, braid, and tangle theory appropriate to chemistry and molecular str

285 Further, the march of neurofibrillary tangles through brain circuits appears to take advantage

286 Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and

287 ution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is cri

288 equivalent loads of amyloid-beta plaques and tangles to those found in demented Alzheimer's cases wit

289 ently of their accumulation into plaques and tangles, to drive healthy neurons into the diseased stat

290 -mortem Braak staging of neurofibrillary tau tangle topographical distribution is one of the core neu

291 er's neuropathology (amyloid plaques and tau tangles) using a postmortem sample of healthy, mild cogn

292 characterized by focal lesions of enlarged, tangled vessels that shunt blood from arteries directly

293 Brainstem tangles were associated with more depressive symptoms in

294 and beta-amyloid (Abeta) and neurofibrillary tangles were identified by immunohistochemistry and quan

295 eyes, leakage was noted in 1 eye, shunts and tangles were noted in 3 eyes, and macular abnormalities

296 h the formation of UCH-L1-immunoreactive tau tangles, whereas UCH-L1(M) has been implicated in alpha-

297 with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by inter

298 cells and thus their evolution is inexorably tangled with host biology.

299 heimer's disease and diffuse neurofibrillary tangles with calcification, characterized by accumulatio

300 ted intense labelling of non-ghost and ghost tangles with PBB3 and AV-1451, while dystrophic neurites